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. 2021 Jan 1;11(4):1609–1625. doi: 10.7150/thno.48153

Figure 3.

Figure 3

Endothelial KLF2 mediates the inhibitory effects of simvastatin on TAC-induced cardiac myofibroblast formation and fibroblast proliferation. A-D, Simvastatin decreases ɑ-SMA positive myofibroblast formation (A), reduces cardiac fibroblast proliferation shown by proliferating cell nuclear antigen (PCNA)/Vimentin (Vim) coimmunostaining (B) in TAC heart compared with the vehicle control, with no significant change in the sham mice (n=10). Simvastatin also reduced the and expression of α-SMA and collagen I (COL I), III (COL III) by western blot (C) and other extracellular matrix genes including vimentin (Vim), fibronectin (Fn), collagen type I alpha 1 subunit (Col1a1), collagen type III alpha 1 subunit (Col3a1) by RT-qPCR (n=5). (D) E-H, RGD-nanoparticle in vivo inhibition of EC-Klf2 expression reverses the simvastatin-mediated reduced α-SMA positive myofibroblasts (E), fibroblast proliferation (F), and the reduced expression of fibrotic genes, collagen type I, III by western blot (G) as well as other extracellular matrix genes by RT-qPCR (H) (n=5-10). Data are means ± S.E.M. *P<0.05, **P<0.01 and n.s not significant. 2-way ANOVA with Turkey test. Scale bars: A, B, E, F, 50 µm.